ライフサイエンスコーパス: tuberculous

1 ie Kinder der Tuberkuloesen (Children of the Tuberculous).

2 illi in the lung and spleen after a virulent tuberculous aerosol challenge.

3 fluid and plasma to differentially diagnose tuberculous and malignant pleural effusion.

4 Recovery of the tuberculous and nontuberculous isolates by the Tween 80-

5 Recovery of the tuberculous and nontuberculous mycobacteria following CB

6 trument-negative MGIT cultures included both tuberculous and nontuberculous mycobacteria.

7 ell surface molecules present in several non-tuberculous and opportunistic mycobacterial species.

8 Tuberculous and postoperative infections were excluded.

9 entify and differentiate between features of tuberculous and pyogenic spondylodiscitis on MR images.

10 es of lymph node cells from protein-deprived tuberculous animals.

11 Their intriguing conservation in pathogenic tuberculous bacteria and the fact that these highly immu

12 , serofibrinous, and fungoid forms), whereas tuberculous bursitis exhibited two patterns of involveme

13 ree cows, 3 Mycobacterium bovis BCG-infected tuberculous cattle, or 3 cows artificially inoculated wi

14 5B-immunized mice (305 +/- 9 days) after the tuberculous challenge was extended 102 days relative to

15 eting cells, and significant resistance to a tuberculous challenge.

16 escribes a novel PPD protein present only in tuberculous complex mycobacteria.

17 contribute to the granulomatous response in tuberculous diseases.

18 of DILI were acetaminophen (35.0 %) and anti-tuberculous drugs (34.7 %).

19 hat cares for about 200 patients with active tuberculous each year.

20 t include background immunity induced by non-tuberculous environmental mycobacteria, diversity of BCG

21 In the tuberculous granulation tissue surrounding caseous and l

22 sential for maintaining the structure of the tuberculous granuloma and may regulate the granulomatous

23 Thus, TNF is not required for tuberculous granuloma formation, but maintains granuloma

24 t and consequences of vascularization of the tuberculous granuloma in the zebrafish-Mycobacterium mar

25 TNF results in marked disorganization of the tuberculous granuloma, as demonstrated by the dissolutio

26 gs about the composition and dynamics of the tuberculous granuloma, the central host structure in myc

27 n, and are amplified and disseminated by the tuberculous granuloma.

28 cted macrophages undergoing apoptosis in the tuberculous granuloma.

29 erates macrophage recruitment to the forming tuberculous granuloma.

30 le in modulating the cellular composition of tuberculous granuloma; 2) CXCR3 impairs antimycobacteria

31 What is happening inside the tuberculous granuloma?

32 is essential for the formation of protective tuberculous granulomas and regulates the expression of o

33 he observed patterns of neutrophils in human tuberculous granulomas and the susceptibility of humans

34 Tuberculous granulomas have long been considered host-pr

35 this probe to evaluate the oxygen tension in tuberculous granulomas in four animal models of disease:

36 eity of local immunologic characteristics of tuberculous granulomas in nonhuman primates.

37 Immunity, Egen et al. present live images of tuberculous granulomas of the mouse, demonstrating the i

38 Zebrafish tuberculous granulomas undergo caseous necrosis, similar

39 e functional consequences of angiogenesis in tuberculous granulomas, and data that balanced inflammat

40 tly elevated in the inflammatory zone of the tuberculous granulomas, and in the nongranulomatous pneu

41 le in both the construction and breakdown of tuberculous granulomas, our results suggest that TDM may

42 rious conditions postulated to be operant in tuberculous granulomas, suggesting that their granuloma-

43 Although tuberculous granulomas, which are composed of infected m

44 In contrast to mammalian tuberculous granulomas, zebrafish lesions contain few ly

45 ing persistence in mycobacteria-which models tuberculous granulomas-are partly determined by a mechan

46 s undergo caseous necrosis, similar to human tuberculous granulomas.

47 he functional capacity of these cells within tuberculous granulomas.

48 d NO are present in specialized areas of the tuberculous granulomas; their precise role in human TB r

49 Since apoptosis is observed in tuberculous granulomata, we investigated the molecular m

50 Malnourished, tuberculous guinea pigs harbored only 20 and 60% of the

51 Hepatobiliary tuberculosis includes miliary, tuberculous hepatitis or localized forms.

52 individuals who had radiographic evidence of tuberculous infection (i.e., calcified granulomas) were

53 the contributions of reactivation of latent tuberculous infection (LTBI) and the progression of new

54 tor from such countries increase the risk of tuberculous infection among young children.

55 veillance data concerning groups at risk for tuberculous infection and allows recommended public heal

56 mportant measures for interpreting trends in tuberculous infection and disease but are complicated by

57 itis C and graft failure without evidence of tuberculous infection at death.

58 Reactivation of latent tuberculous infection by aminoguanidine treatment was co

59 t RNI are required for the control of murine tuberculous infection caused by both laboratory and clin

60 The annual risk of tuberculous infection for white men in the United States

61 To assess whether there is increased risk of tuberculous infection in children who traveled to or had

62 The outcome of tuberculous infection in mice deficient in the CD11b sub

63 nd incentive approaches, treatment of latent tuberculous infection in those HIV-seropositive, and scr

64 tion-based national data are available about tuberculous infection in young people from such backgrou

65 is not useful in screening for asymptomatic tuberculous infection or for diagnosing active tuberculo

66 A case of tuberculous infection was defined as a positive tubercul

67 The incidence of tuberculous infection was measured in a cohort of 8809 c

68 mechanisms involved in the control of latent tuberculous infection were examined using two murine exp

69 In an at-risk population for tuberculous infection who were either tuberculin skin te

70 are important for containing and restricting tuberculous infection, and suggest that malnutrition-ind

71 In a setting with a high risk of tuberculous infection, HIV-1 increases the risk of recur

72 The secondary outcome was the incidence of tuberculous infection, measured using tuberculin skin te

73 importance of Th1 immunity in the control of tuberculous infection, the results of the present study

74 p with a high prevalence of tuberculosis and tuberculous infection, these efforts remain an important

75 cines in cattle, a natural target species of tuberculous infection.

76 morphological features with persistent human tuberculous infection.

77 city of the test depended on the presence of tuberculous infection.

78 phage activation in controlling a persistent tuberculous infection.

79 ar cells from persons across the spectrum of tuberculous infection.

80 ity has a high positive predictive value for tuberculous infection.

81 tified by country and baseline prevalence of tuberculous infection: group 1 strengthened tuberculosis

82 on disease progression in mice with chronic tuberculous infections.

83 tral role that CD4 cells play in controlling tuberculous infections.

84 the host in both persistent and reactivated tuberculous infections.

85 this therapeutic approach markedly inhibits tuberculous inflammation in lungs, increases the surviva

86 smigration across pleural mesothelium during tuberculous inflammation was investigated.

87 Recovery of the tuberculous isolates following NALC-NaOH processing aver

88 are as follows: growth of MDR TB from an old tuberculous lesion in a patient who was never treated fo

89 Liquefaction of solid caseous tuberculous lesions and the subsequent cavity formation

90 PSMA PET-positive lung cancers as well as in tuberculous lesions from our histologic database.

91 both macrophage physiology and the nature of tuberculous lesions in man and animals suggests that hyp

92 The 2 tuberculous lesions showed an SUVmax of 7.8 and 2.5.

93 lymphocytes and immature macrophages in the tuberculous lung are basic to the local immunopathogenes

94 found in the affected but not the unaffected tuberculous lung compared with healthy controls.

95 ons associated with B cell-rich foci seen in tuberculous lung granulomas.

96 F-alpha) was also significantly increased in tuberculous lungs and was principally localized to the n

97 e in controlling TB, its expression in human tuberculous lungs has not been systematically characteri

98 Tuberculous lymphadenitis (TBL) is the most common form

99 inal failure, mutations in the NOD2 gene and tuberculous lymphadenitis has not been described before.

100 Tuberculous lymphadenitis is the main manifestation of e

101 evidence proved or was highly suggestive for tuberculous lymphadenitis.

102 in 2002 will have prevented 29,729 cases of tuberculous meningitis (5th-95th centiles, 24,063-36,192

103 e cerebrospinal fluid (CSF) of patients with tuberculous meningitis (TBM) are associated with TBM-IRI

104 Point-of-care tests for tuberculous meningitis (TBM) are needed.

105 Murine models of tuberculous meningitis (TBM) have not reflected the seve

106 Tuberculous meningitis (TBM) is a devastating form of tu

107 Tuberculous meningitis (TBM) is a frequent cause of meni

108 Tuberculous meningitis (TBM) is a severe complication of

109 Drug-resistant tuberculous meningitis (TBM) is difficult to diagnose an

110 Tuberculous meningitis (TBM) is the most devastating for

111 Tuberculous meningitis (TBM) is the most severe form of

112 Tuberculous meningitis (TBM) leads to death or disabilit

113 Tuberculous meningitis (TBM) remains a major cause of de

114 Tuberculous meningitis (TBM) research is hampered by low

115 Early diagnosis and treatment of tuberculous meningitis (TBM) saves lives, but current la

116 a national molecular diagnostic service for tuberculous meningitis (TBM) using an in-house IS6110-ta

117 ibute to the high morbidity and mortality of tuberculous meningitis (TBM), but the link between infla

118 e available on their use in the diagnosis of tuberculous meningitis (TBM).

119 udy of HIV-infected, ART-naive patients with tuberculous meningitis (TBM).

120 Tuberculous meningitis (TM) is difficult to diagnose and

121 diagnosis; the rest had probable or possible tuberculous meningitis according to published criteria.

122 We calculated the number of tuberculous meningitis and miliary tuberculosis cases th

123 consistently high efficacy against childhood tuberculous meningitis and miliary tuberculosis, but var

124 The polymorphisms were associated with both tuberculous meningitis and pulmonary tuberculosis and we

125 lware discusses the challenges of diagnosing tuberculous meningitis and the implications of the study

126 ants were classified as probable or definite tuberculous meningitis by uniform case definition, exclu

127 87; 16 of 23 cases) for probable or definite tuberculous meningitis compared with 43% (23-66; 10/23)

128 6 in cerebrospinal fluid leukocytes improves tuberculous meningitis diagnosis.

129 Tuberculous meningitis disproportionately affects young

130 Despite treatment, childhood tuberculous meningitis has very poor outcomes.

131 With composite standard, we detected tuberculous meningitis in 22 (17%) of 129 participants.

132 Laboratory evidence for tuberculous meningitis is difficult to acquire due to th

133 Tuberculous meningitis is especially common in young chi

134 design in Vietnam with cases that had either tuberculous meningitis or pulmonary tuberculosis.

135 search that were drafted at an international tuberculous meningitis research meeting organized by the

136 ematic review and meta-analysis of childhood tuberculous meningitis studies published up to Oct 12, 2

137 and low threshold for empirical treatment of tuberculous meningitis suspects.

138 ION: Xpert Ultra detected significantly more tuberculous meningitis than did either Xpert or culture.

139 higher rate of survival among patients with tuberculous meningitis than standard treatment.

140 Here, we use a rabbit model of tuberculous meningitis to evaluate the severity of disea

141 Tuberculous meningitis was observed in animals given M.

142 o hundred and eighty patients with suspected tuberculous meningitis were enrolled.

143 usly reported that rabbits with experimental tuberculous meningitis were protected from death by a co

144 fluid specimens from patients with suspected tuberculous meningitis were stained by conventional Zieh

145 infected adults with a clinical diagnosis of tuberculous meningitis who were admitted to one of two V

146 The pathogenesis of tuberculous meningitis, a devastating complication of tu

147 t approaches to prevent, diagnose, and treat tuberculous meningitis, and there are still too few answ

148 le tuberculous meningitis, three as possible tuberculous meningitis, and two as not tuberculous menin

149 ds are recommended as adjunctive therapy for tuberculous meningitis, the mechanism underlying their b

150 In tuberculous meningitis, the polymorphism is associated w

151 se eight, three were categorised as probable tuberculous meningitis, three as possible tuberculous me

152 Using a rabbit model of tuberculous meningitis, we evaluated the protective effi

153 as the initial diagnostic test for suspected tuberculous meningitis.

154 he new Xpert MTB/RIF Ultra (Xpert Ultra) for tuberculous meningitis.

155 rt MTB/RIF as initial diagnostic testing for tuberculous meningitis.

156 sible tuberculous meningitis, and two as not tuberculous meningitis.

157 ar stain improve the laboratory diagnosis of tuberculous meningitis.

158 ct of PDE-Is on the duration of treatment in tuberculous mice.

159 cilomilast accelerated the time to death in tuberculous mice.

160 finding that sequences representative of non-tuberculous mycobacteria (NTM) and other opportunistic h

161 Non-tuberculous mycobacteria (NTM) are a large family of aci

162 teria, the four-gene module occurred only in tuberculous mycobacteria and was required for intramacro

163 Non-tuberculous mycobacteria cause a broad range of clinical

164 itive diagnostic assays for the detection of tuberculous mycobacteria in elephants are lacking.

165 ence of tuberculosis and infections with non-tuberculous mycobacteria in human populations, but the m

166 Despite concerns about non-tuberculous mycobacteria, especially Mycobacterium absce

167 cid biosynthesis, is very potent against the tuberculous mycobacteria.

168 Pulmonary non-tuberculous mycobacterial (NTM) disease epidemiology in

169 Furthermore, isolated pulmonary non-tuberculous mycobacterial infection has been increasing

170 to confer susceptibility to disseminated non-tuberculous mycobacterial infection.

171 Cultures suggestive of Non-tuberculous mycobacterial infections (NTM) were sub-cult

172 actors underlying localised and systemic non-tuberculous mycobacterial infections.

173 ng infected with the multidrug-resistant non-tuberculous mycobacterium (NTM) Mycobacterium abscessus,

174 which has a smooth colony morphology, is the tuberculous organism retaining the most genetic traits f

175 He found that children of tuberculous parents had higher mortality rates and lower

176 control tuberculosis, leprosy and other non-tuberculous pathogens.

177 To identify host cell genes involved in tuberculous pathology, we screened macrophage cDNA libra

178 d IL-1 beta, was not up-regulated in PBMC of tuberculous patients.

179 , NF-kappa B was activated in monocytes from tuberculous patients.

180 14 of 28 specimens (50%) from patients with tuberculous pericarditis (P > 0.15).

181 fluid (PF) lipoarabinomannan (LAM) assays in tuberculous pericarditis (TBP).

182 Sixteen of the 20 patients had tuberculous pericarditis and 4 patients had other diagno

183 30 of 43 specimens (70%) from patients with tuberculous pericarditis and by PCR in 14 of 28 specimen

184 ture and histopathology for the diagnosis of tuberculous pericarditis in 36 specimens of pericardial

185 Tuberculous pericarditis is associated with high morbidi

186 signed 1400 adults with definite or probable tuberculous pericarditis to either prednisolone or place

187 In patients with tuberculous pericarditis, neither prednisolone nor M. in

188 le diseases such as rheumatic heart disease, tuberculous pericarditis, or cardiomyopathy and others h

189 ndicus pranii immunotherapy in patients with tuberculous pericarditis.

190 -characterized ascitic fluid bank, including tuberculous peritonitis (n = 7), tuberculous peritonitis

191 of ascitic fluid ADA activity in diagnosing tuberculous peritonitis in a U.S. patient population.

192 , including tuberculous peritonitis (n = 7), tuberculous peritonitis in the setting of cirrhosis (n =

193 ver, ADA was only 30% sensitive in detecting tuberculous peritonitis in the setting of cirrhosis, and

194 sis, and cirrhosis was present in 59% of the tuberculous peritonitis patients in our population.

195 ivity of the ADA determination in diagnosing tuberculous peritonitis was only 58.8%, and the specific

196 Tuberculous peritonitis, although common in Third World

197 We enrolled 91 cases, including tuberculous pleural effusion (TPE, n = 50), malignant pl

198 s facilitates monocyte transmigration during tuberculous pleural inflammation.

199 tributed, being more common in patients with tuberculous pleurisy (92%) in comparison with healthy M.

200 Tuberculous pleurisy is a severe inflammatory response i

201 Analysis of cytokine expression during tuberculous pleurisy may lead to a better understanding

202 In tuberculous pleurisy pleural mesothelial cells are expos

203 We have used the guinea pig model of tuberculous pleurisy to examine several aspects of the i

204 by using the established guinea pig model of tuberculous pleurisy.

205 in pleural biopsy sections of patients with tuberculous pleurisy.

206 f pleural macrophages in the pathogenesis of tuberculous pleuritis and to monitor the response to ant

207 hages play critical roles in pathogenesis of tuberculous pleuritis, but very little is known about th

208 l mesothelial cells (PMCs) express ICAM-1 in tuberculous pleuritis.

209 reater than those of PBMC from patients with tuberculous pleuritis.

210 owing antibiotics treatment in patients with tuberculous pleuritis.

211 t mechanisms contribute to the prevention of tuberculous reactivation.

212 ry tuberculosis compared with those with non-tuberculous respiratory tract infections.

213 o be infected, with up to 8% having external tuberculous signs, in wild populations in Northumberland

214 diagnosed with pyogenic spondylodiscitis and tuberculous spondylodiscitis allowed identification of i

215 regarding possibility to distinguish between tuberculous spondylodiscitis and pyogenic spondylodiscit

216 Prevailing features of tuberculous spondylodiscitis included: involvement of th

217 Tuberculous spondylodiscitis is characterized by the loc

218 with pyogenic spondylodiscitis, and 16 with tuberculous spondylodiscitis).

219 Transient worsening of tuberculous symptomatology and lesions following antitub

220 okine that is implicated in the formation of tuberculous (TB) granulomas and in immunity to Mycobacte

221 R imaging allowed evaluation of all forms of tuberculous tenosynovitis (hygromatous, serofibrinous, a

222 Tuberculous tenosynovitis most commonly involved the ten

223 All cases of tuberculous tenosynovitis or bursitis showed soft-tissue

224 Twelve patients had tuberculous tenosynovitis, and nine had bursitis.

225 osite reference standard of any positive CSF tuberculous test.

226 y more accurate in identifying true-positive tuberculous uveitis cases than was T-SPOT.TB among disco

227 and the tuberculin skin test) for diagnosing tuberculous uveitis.

228 red for assessment of the efficiency of anti-tuberculous vaccines.

229 meningitis (TBM) is the most severe form of tuberculous with substantial mortality.